Discovery promises to make retina, spinal cord and other central
nervous system transplants possible

BOSTON, April 26, 2007 /PRNewswire/ -- Scientists at the
Schepens Eye Research Institute, an affiliate of Harvard Medical
School, have identified a key mechanism for successfully
transplanting tissue into the adult central nervous system. The
study found that a molecule known as MMP-2 (which is induced by
stem cells) has the ability to break down barriers on the outer
surface of a damaged retina and allow healthy donor cells to
integrate and wire themselves into remaining recipient tissue. The
finding, reported in the current issue (April 25, 2007) of the
Journal of Neuroscience, holds great promise not only for patients
with retinal disease, but also for those suffering from spinal cord
injuries and neurodegenerative disorders such as Parkinson's and
Alzheimer's Diseases.

"This is a very significant finding," says Dr. Michael Young,
associate scientist at the Schepens Eye Research Institute and
principal investigator of the study. "We believe that it will
ultimately make retinal transplantation and restoration of vision a
possibility." He adds that transplantation of donor photoreceptors
(in whole retina transplants) may prove to be more beneficial than
transplanting stem cells alone, as these retinal transplants
contain a complete organized supply of cells necessary for proper
vision.

The regenerative capacity of central nervous system tissue in
adult mammals, including human begins, is extremely limited. This
is partly due to the formation of barriers, known as "glial" scars,
which are triggered by the body to protect the injured retina or
other nerve tissue from further damage. This dense scar tissue
throws up a blockade to foreign cells, including transplants meant
to heal and regenerate. This is what has made previous attempts to
transplant whole donor retinas so difficult, according to
Young
.

On the other hand, in recent years, stem cells have been shown
to overcome these physical barriers, easily penetrating the scar
and integrating into the injured tissue.

For instance, in studies published several years ago, Young and
his colleagues demonstrated this special stem-cell talent in
damaged mouse retinas. In those studies cells injected into injured
retinas quickly integrated into the existing retinal tissue.

Intrigued by this phenomenon, Young and his team believed that
if they could identify and harness the key molecules used by stem
cells to gain access into the injured retina, they could
potentially improve the success of non- stem cell transplants.
Based on this idea, the team conducted a series of experiments.

In their initial experiments, the team compared the chemicals
that were generated when stem cells were injected into damaged
retinas and those produced when they attempted to transplant whole
retina tissue into the eyes of mice with degenerated retinas. They
found-in the stem cell injected retinas-an increase in the amount
of and the level of activity of the molecule MMP-2 in host tissue.
They concluded that this molecule dissolved the scar on the outer
surface of the retina. There was no increase in MMP-2 when they
attempted whole-retina transplants.

The team went on to transplant a layer of stem cells between the
degenerating mice retinas and healthy donor tissue (whole retina).
They found that MMP-2 induced removal of the scar barrier and
allowed healthy donor cells (of the whole retina) to make new
connections with the damaged retinas in the mice.

"These are very powerful results," says Young. "We are convinced
that the increase of this molecule is a major key to creating a
permissive environment for central nervous system
regeneration."

The team is now investigating therapeutic approaches that would
eliminate the need for stem cells. This would involve the use of
just the MMP-2 molecule, w
hich is already available in the
pharmaceutical market, to foster a receptive transplant environment
in the eye, and, in other CNS tissues.

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